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1.
H Hayashi T Yoshimura J Y Chen 《Comparative immunology, microbiology and infectious diseases》1985,8(2):73-87
Our particular attention in this article was given to natural mediators for macrophages isolated from the sites of tissue injury. A number of chemotactic factors, which may satisfy many criteria making them acceptable as inflammatory leucocyte chemotactic factors, has been separated. Among them, our laboratory has isolated three macrophage (monocyte) chemotactic factors (MCF-a, -b and -c). Their purification, characterization and functional specificity are discussed. 相似文献
2.
A Caignard P Lagadec D Reisser J F Jeannin M S Martin F Martin 《Comparative immunology, microbiology and infectious diseases》1985,8(2):147-157
The capability of activated macrophages to kill tumor cells in vitro is now well documented. The tumoricidal activation of macrophages against intestinal tumor cells by different agents is described and the main hypothesis on the mechanisms of tumor cell killing in vitro are discussed. These in vitro results suggest that the macrophage can constitute an efficient effector cell in the defense against intestinal tumors. The distribution and ratio of macrophages in normal intestine and intestinal tumors is described. At the moment, potent activators of macrophages studied in vivo on experimental and human intestinal tumors give poor results or even enhance the growth of tumors. Macrophages may also interfere with the specific immune response in two directions by enhancing the immune response or decreasing it by elaboration of mediators such as prostaglandins. 相似文献
3.
Reasons for performing study: There is increasing evidence of involvement of inflammatory cells in acute laminitis. Objective: To immunolocalise monocytes/macrophages and B and T lymphocytes in the laminar tissue of normal horses and those with black walnut extract (BWE)‐induced laminitis. Methods: Immunohistochemistry was used in archived laminar tissue samples from 20 horses divided equally into 4 groups: control animals (CON), and those administered BWE at 1.5 h (1.5H DTP group), at the onset of leucopenia (3H DTP group) and at the onset of lameness (LAM group). Antibodies against CD3, CD20 and CD163 were used to recognise lymphocytes (T and B) and monocytes/macrophages, respectively. Results: Mononuclear cells were present in laminar tissue of normal horses. The majority of CD3‐ and CD20‐positive lymphocytes were localised around the deep dermal vessels but were also evident around vessels of the primary dermal laminae. CD163‐positive macrophages were primarily perivascular in deep dermis or in dermal laminae. No changes in the number of laminar B or T lymphocytes occurred at any time point post BWE administration. However, increases (P = 0.0016) in laminar CD163‐positive cells occurred in the secondary dermal laminae (SDL) in the 1.5H DTP and 3H DTP groups, returning to basal values in LAM group. Conclusions: Lymphocyte and macrophage populations are present in the laminar tissue of clinically normal horses and BWE administration induces an increase in CD163‐positive macrophages in SDL. Potential relevance: Both the host tissue population of mononuclear cells and the influx of monocytes may play an important role in the pathophysiological changes leading to laminar injury. 相似文献
4.
During infection and inflammation drug disposition and hepatic metabolism are markedly affected in mammals. Pro-inflammatory mediators play an important role in the suppression of (cytochrome-P450-mediated) drug metabolism. Inflammatory mediators like cytokines, nitric oxide (NO), reactive oxygen species (ROS) and eicosanoids are released by activated macrophages from various sources, including liver and lung. It was the aim of this study to investigate ways to suppress the activation of macrophages during the onset of the inflammatory cascade. Therefore porcine lung and liver macrophages were isolated, and incubated with lipopolysaccharide (LPS) to initiate an acute inflammatory response, represented by the release of high amounts of tumour necrosis factor-alpha (TNF-alpha) into the culture medium. Additionally the primary macrophages were coincubated with phosphodiesterase-IV-(PDE-IV)-inhibitors or beta-adrenoceptor agonists that in previous studies demonstrated strong suppressive effects on TNF-alpha release. Especially the beta-adrenoceptor agonists showed to be very potent TNF-alpha suppressants, which indicates that the beta-adrenoceptor might be an interesting target for suppression of activation of macrophages. This was strengthened by the observation that the beta-adrenoceptor expression was not altered during the onset of the inflammatory cascade. 相似文献
5.
Todd C. Duffy DVM Rebecca Kirby DVM DACVIM DACVECC Elke Rudloff DVM DACVECC 《Journal of Veterinary Emergency and Critical Care》2004,14(2):84-99
Objective: To review the human and veterinary literature on the role of the vascular endothelial cell in health, as well as during hypoxic and inflammatory disease states. Data sources: Data from human and veterinary literature were reviewed through a Pubmed search and a manual search of the references listed in articles covering some aspect of vascular endothelial cell function. Human data synthesis: The development of techniques that allow the maintenance and growth of endothelial cells in culture has produced an explosion of new research in the area of endothelial cell physiology. This plethora of data has revealed the critical role that vascular endothelial cells play in both health and disease states. Interspecies variations can occur with respect to the vascular endothelial cell physiology and its response to pathologic conditions. Veterinary data synthesis: There is a paucity of information regarding the role of the vascular endothelial cell in health or disease of small animals. Many human studies use species cared for by veterinarians, providing information that may be applied to small animals and that may be used to construct future studies. Conclusion: An organ system itself, the vascular endothelium is an essential component of all organs in the body. The endothelial cell lining functions to maintain selective permeability between the blood and the tissue it supplies, regulate vascular tone, sustain blood fluidity through regulation of coagulation, and modulate interaction of leukocytes with the interstitium and inflammatory reactions. During disease states, the endothelial cell functions locally to limit the boundaries of the disease process. If these functions are not controlled, they can become a part of the pathogenic process, contributing to blood stasis and thrombosis, potentiation of local inflammation and interstitial edema formation, subsequent tissue hypoxia, and multiple organ dysfunction. Pharmacological investigations targeting the modulation of endothelial function during disease states have not yet advanced treatment protocols. Since all critically ill animals are at risk for some degree of endothelial cell dysfunction, treatment regimens should focus on promoting capillary blood flow and tissue oxygen delivery. 相似文献
6.
To date, there is a substantial amount of data to support the hypotheses that vascular and enzymatic changes are ongoing in experimental laminitis. Furthermore, there is substantial in vitro evidence that the enzymatic changes weaken the dermo-epidermal attachments leading to mechanical failure of the hoof-bone interface of the equine digit. However, investigators of both the vascular and enzymatic theories have, to date, been unable to substantiate the effects of these pathophysiological changes in vivo on laminar tissues of horses afflicted with experimentally induced or naturally acquired laminitis. In addition, the effects of laminitis-inducing treatment have not been prevented or reversed by treatment with an MMP inhibitor or a vasoactive antagonist. It is possible that there is simultaneous activation of the vascular and enzymatic pathways and/or other inflammatory processes. Moreover, the third theory involving mechanical factors cannot be discounted simply because strong evidence for vascular and enzymatic changes exists. It is common for horses with severe musculoskeletal disease affecting weightbearing on a limb to develop laminitis in the contralateral limb. It remains to be determined what factors are responsible for initiation of laminitis in these individuals. Evidence has not been presented that precludes the possibility of coincident occurrence of vascular and enzymatic changes. In fact, many of the inflammatory mediators (e.g. interleukin-1beta) found in laminitic tissues can concurrently stimulate synthesis of vasoactive substances and activate MMPs. Because enzymatic action on proteins is largely dependent on the concentrations of proteins and enzyme, the enzymatic theory is not dependent upon increased delivery of enzymes via increased capillary flow. Likewise, because vascular changes can alter tissue function via increased capillary flow and oedema formation, the vascular theory is not dependent upon decreased capillary flow. It is true that naturally acquired laminitis is widely variable in severity and predisposing diseases. Therefore, most probably there are multiple mechanisms involved in the initiation and propagation of the pathophysiologic cascade(s) and, therefore, successful intervention will necessitate multiple treatment modalities. 相似文献
7.
M. Guenounou F. Vacheron C. Nauciel 《Comparative immunology, microbiology and infectious diseases》1985,8(3-4):273-284
Bacterial peptidoglycans and the synthetic analog muramyl dipeptide possess various immunomodulating properties (adjuvant effect, increase of resistance to infectious agents and to tumor growth). They are able to induce B cell activation and to stimulate macrophages to produce monokines such as Interleukin 1 (IL 1). IL 1 plays an essential role in immune response. It promotes thymocytes maturation and Interleukin 2 secretion by antigen sensitive T cells, which in turn triggers regulatory T cells. Moreover, it is involved in the proliferation and differentiation of B cells.
There is a correlation between the immunoenhancing effect of PG of a definite structure and their ability to induce IL 1 secretion. Non-adjuvant PG were inactive. This suggests that one of the major mechanisms of action of adjuvant PG could be the stimulation of IL 1 synthesis. 相似文献
8.
9.
Concepci��n Revilla Teresa Poderoso Paloma Mart��nez Bel��n ��lvarez Laura L��pez-Fuertes Fernando Alonso Angel Ezquerra Javier Dom��nguez 《Veterinary research》2009,40(3)
Antibody-mediated targeting of antigen to specific antigen presenting cells (APC) receptors is an attractive strategy to enhance T cell immune responses to weak immunogenic antigens. Here, we describe the characterization of two monoclonal antibodies (mAb) against different epitopes of porcine sialoadhesin (Sn) and evaluate in vitro the potential of targeting this receptor for delivery of antigens to APC for T cell stimulation. The specificity of these mAb was determined by amino acid sequence analysis of peptides derived from the affinity purified antigen. Porcine Sn is expressed by macrophages present in the border between white and red pulp of the spleen and in the subcapsular sinus of lymph nodes, an appropriate location for trapping blood and lymph-borne antigens. It is also expressed by alveolar macrophages and monocyte-derived dendritic cells (MoDC). Blood monocytes are negative for this molecule, but its expression can be induced by treatment with IFN-a. MAb bound to Sn is rapidly endocytosed. MAb to sialoadhesin induced in vitro T cell proliferation at concentrations 100-fold lower than the non-targeting control mAb when using T lymphocytes from pigs immunized with mouse immunoglobulins as responder cells and IFN-a treated monocytes or MoDC as APC, suggesting a role of sialoadhesin in antigen uptake and/or delivery into the presentation pathway in APC. 相似文献
10.
11.
Activation of macrophages 总被引：2，自引：0，他引：2
The role of macrophages is essential in the development of a normal immune response. Not only are these cells involved in the initiation of this response by presenting antigens to lymphocytes and by producing Interleukin I, but they also participate in the various phenomena of cellular co-operation and regulation. It is also evident that macrophages can act as cytotoxic effector cells, especially against micro-organisms and tumor cells. This last function is restricted to activated macrophages. The aim of this review is to summarize our present knowledge concerning this "macrophage activation". 相似文献
12.
ABSTRACT: Porcine reproductive and respiratory syndrome virus (PRRSV) is an arterivirus that shows a restricted in vivo tropism for subsets of porcine macrophages, with alveolar macrophages being major target cells. The virus is associated with respiratory problems in pigs of all ages and is commonly isolated on farms with porcine respiratory disease complex (PRDC). Due to virus-induced macrophage death early in infection, PRRSV hampers the innate defence against pathogens in the lungs. In addition, the virus might also directly affect the antimicrobial functions of macrophages. This study examined whether interaction of European genotype PRRSV with primary alveolar macrophages (PAM) affects their phagocytic capacity. Inoculation of macrophages with both subtype I PRRSV (LV) and subtype III PRRSV (Lena) showed that the virus inhibits PAM phagocytosis. Similar results were obtained using inactivated PRRSV (LV), showing that initial interaction of the virion with the cell is sufficient to reduce phagocytosis, and that no productive infection is required. When macrophages were incubated with sialoadhesin- (Sn) or CD163-specific antibodies, two entry mediators of the virus, only Sn-specific antibodies downregulated the phagocytic capacity of PAM, indicating that interaction with Sn, but not CD163, mediates the inhibitory effect of PRRSV on phagocytosis. In conclusion, this study shows that European genotype PRRSV inhibits PAM phagocytosis in vitro, through the interaction with its internalization receptor Sn. If similar events occur in vivo, this interaction may be important in the development of PRDC, as often seen in the field. 相似文献
13.
Sharon Elazar Erez Gonen Ayala Livneh-Kol Ilan Rosenshine Nahum Yehuda Shpigel 《Veterinary research》2010,41(1)
Mastitis, inflammation of the mammary tissue, is a common disease in dairy animals and mammary pathogenic Escherichia coli (MPEC) is a leading cause of the disease. Lipopolysaccharide (LPS) is an important virulence factor of MPEC and inoculation of the mammary glands with bacterial LPS is sufficient to induce an inflammatory response. We previously showed using adoptive transfer of normal macrophages into the mammary gland of TLR4-deficient C3H/HeJ mice that LPS/TLR4 signaling on mammary alveolar macrophages is sufficient to elicit neutrophil recruitment into the alveolar space. Here we show that TLR4-normal C3H/HeN mice, depleted of alveolar macrophages, were completely refractory to LPS intramammary challenge. These results indicate that alveolar macrophages are both sufficient and essential for neutrophil recruitment elicited by LPS/TLR4 signaling in the mammary gland. Using TNFα gene-knockout mice and adoptive transfer of wild-type macrophages, we show here that TNFα produced by mammary alveolar macrophages in response to LPS/TLR4 signaling is an essential mediator eliciting blood neutrophil recruitment into the milk spaces. Furthermore, using the IL8 receptor or IL1 receptor gene-knockout mice we observed abrogated recruitment of neutrophils into the mammary gland and their entrapment on the basal side of the alveolar epithelium in response to intramammary LPS challenge. Adoptive transfer of wild-type neutrophils to IL1 receptor knockout mice, just before LPS challenge, restored normal neutrophil recruitment into the milk spaces. We conclude that neutrophil recruitment to the milk spaces is: (i) mediated through TNFα, which is produced by alveolar macrophages in response to LPS/TLR4 signaling and (ii) is dependent on IL8 and IL1β signaling and regulated by iNOS-derived NO. 相似文献
14.
Sarah Costers David J. Lefebvre Bruno Goddeeris Peter L. Delputte Hans J. Nauwynck 《Veterinary research》2009,40(5)
The replication of porcine reproductive and respiratory syndrome virus (PRRSV) in lungs and lymphoid tissues of PRRSV-infected pigs is already strongly reduced before the appearance of neutralizing antibodies, indicating that other immune mechanisms are involved in eliminating PRRSV at those sites. This study aimed to determine whether PRRSV Lelystad virus (LV)-specific cytotoxic T-lymphocytes (CTL) can efficiently eliminate PRRSV-infected alveolar macrophages. Therefore, CTL assays were performed with PRRSV-infected alveolar macrophages as target cells and autologous peripheral blood mononuclear cells (PBMC) from PRRSV-infected pigs as a source of PRRSV-specific CTL. PBMC of 3 PRRSV-infected pigs were used either directly in CTL assays, or following restimulation in vitro. CTL assays with pseudorabies virus (PRV) Begonia-infected alveolar macrophages and autologous PBMC, from 2 PRV Begonia-inoculated pigs, were performed for validation of the assays. In freshly isolated PBMC, derived from PRRSV-infected pigs, CTL activity towards PRRSV-infected macrophages was not detected until the end of the experiment (56 days post infection – dpi). Restimulating the PBMC with PRRSV in vitro resulted in proliferation of CD3+CD8high cells starting from 14 dpi. Although CD3+CD8high cells are generally considered to be CTL, CTL activity was not detected in PRRSV-restimulated PBMC of the 3 pigs until 49 dpi. A weak PRRSV-specific CTL activity was observed only at 56 dpi in PRRSV-restimulated PBMC of one pig. In contrast, a clear CTL activity was observed in PRV Begonia-restimulated PBMC, derived from PRV Begonia-infected pigs, starting from 21 dpi. This study indicates that PBMC of PRRSV-infected pigs contain proliferating CD3+CD8high cells upon restimulation in vitro, but these PBMC fail to exert CTL activity towards PRRSV-infected alveolar macrophages. 相似文献
15.
Studies of the response of the primary avian polymorphonuclear leukocyte, the heterophil, to microbe associated molecular patterns (MAMPs) through toll-like receptors (TLR) has concentrated on the activation of the respiratory burst, release of intracellular granules, and the induction of cytokine and chemokine expression. Virtually no studies have been described on the role of lipid mediators, leukotrienes and prostaglandins, as effectors of the avian inflammatory response. We have previously shown that flagellin (FLG), the bacterial lipoprotein mimic palmitoly-3-cysteine-serine-lysine-4 (PAM), and unmethylated CpG motifs of bacteria DNA (CpG) are all potent activators of the avian innate immune system. In the present studies, we hypothesized that FLG, PAM, and CpG are also capable of eliciting the production of these lipid mediators of inflammation by avian heterophils. Compared to non-stimulated control heterophils, all three TLR agonists were potent inducers (3-5-fold increase) of a rapid production (30 min) of leukotriene B(4) (LTB(4)) followed by a later release (60-120 min) of prostaglandin (PGE(2)) by the heterophils. LTB(4) and PGE(2) production were derived from lipoxygenase-5 (5-LO) and cyclooxygenase-2 (COX-2) enzymatic activities, respectively, as the selective 5-LO (caffeic acid) and COX-2 (NS-398) inhibitors eliminated LTB(4) and PGE(2) production from the MAMP-stimulated heterophils. These results demonstrate that both the lipoxygenase and cycloxygenase pathways are operational in avian heterophils in response to bacterial MAMPs. Treatment of heterophils with either FLG, PAM, or CpG also induced a significant increase in DNA binding by NF-κB family members' p50, c-Rel, and RelB. Additionally, the production of LTB(4) and PGE(2) were inhibited following treatment of heterophils with the specific pharmacologic inhibitor of NF-κB (Bay 11-7086), thus suggesting that TLR pathway activation of NF-κB controls LTB(4) and PGE(2) production. This the first report of the production of lipid mediators of inflammation by avian heterophils in response to PAMPs. Since FLG, lipoproteins, and bacterial CpG DNA are abundant during bacterial infections, these data support their role in the inflammatory response mediated by avian heterophils. 相似文献
16.
Fujimoto Y Nakatani N Kubo T Semi Y Yoshida N Nakajima H Iseri T Azuma YT Takeuchi T 《The Journal of veterinary medical science / the Japanese Society of Veterinary Science》2012,74(1):27-34
Macrophages are essential for controlling the majority of infections, and are mediators of natural immunity. During infection, lipopolysaccharide (LPS) stimulates macrophages to produce pro-inflammatory cytokines. Adenosine and ATP released into the extracellular space by immunological stimuli have been shown to regulate various immune functions. More recently, it has been shown adenosine and ATP have a critical role on the physiological negative feedback mechanism for limitation and termination of tissue-specific and systemic inflammatory responses. It was useful and meaningful to gain information about interaction between LPS, which generates the inflammation, and adenosine and ATP, which terminate the inflammation. We evaluate effects of adenosine and ATP on the production of cytokines related to inflammation in canine macrophage cell line DH82 cells. Adenosine and ATP respectively increased the production of IL-10 without affecting the production of IL-6, TNF-α and IL-12 in DH82 cells. In addition, adenosine and ATP prevented the production of LPS-induced IL-6, TNF-α and IL-12 in DH82 cells. In contrast, adenosine and ATP potentiated LPS-induced IL-10 production in DH82 cells. Moreover, adenosine, but not ATP inhibited LPS-induced expression of TLR4 in DH82 cells. These results suggest that conditions related to increased adenosine and/or ATP may play an important role in the inflammatory reactions. 相似文献
17.
综述了国内外蜂胶对非特异性免疫系统的作用及其机理的研究进展,探讨了蜂胶对非特异性免疫反应中各种细胞以及相关免疫介质的影响.研究结果表明:蜂胶能有效提高巨噬细胞、自然杀伤细胞和多形核粒细胞的活性,调节细胞因子的分泌和免疫细胞的增殖,降低巨噬细胞氧化应激反应. 相似文献
18.
Andrade MA Siles-Lucas M López-Abán J Nogal-Ruiz JJ Pérez-Arellano JL Martínez-Fernández AR Muro A 《Veterinary parasitology》2007,143(1):86-90
Trichinellosis is a cosmopolitan zoonotic disease affecting a wide variety of animals, including man. Non-encapsulated and encapsulated species diverge with respect to their developmental strategies. Little is known at the molecular level about parasite-derived mediators responsible for host muscle cell transformation occurring during trichinellosis. In this context, host-parasite relationships in Trichinella-infected animals could be related to different host-immune and cell mediators, e.g. nitric oxide (NO). Here, we investigate the stimulatory/inhibitory role of L1 antigens from four encapsulated (T. spiralis, T. britovi, T. nelsoni and T. nativa) and one non-encapsulated (T. pseudospiralis) Trichinella species on NO production from rat macrophages in vitro. Our results demonstrate that encapsulated and non-encapsulated Trichinella species differ in their capacity to stimulate the secretion of NO from host macrophages. Biological significance of these differences should be further assessed in the available experimental models. 相似文献
19.
P2X7 is an ATP gated purinoceptor that has been linked to various immune responses. P2X7 appears to be expressed ubiquitously in the immune system and thus may be important as an effector pathway or play significant roles in cell activation/death. 2',3'-(4-Benzoyl)benzoyl ATP is the most potent agonist of this receptor and ATP in its fully dissociated form (ATP(4-)) also activates the receptor. High concentrations of ATP can cause the P2X7 receptor to induce pore formation on the surface of the cell that allows molecules of considerable size to pass and can lead to cell death. The P2X7 receptor has also been linked to various immune activities when the concentration of ATP is lower, including the release of IL-1beta. The role P2X7 receptors have on immune cell activities is just beginning to be understood. We sought to determine the role of P2X7 on bovine macrophages in eliminating the causative agent of bovine-type tuberculosis, Mycobacterium bovis. Because high concentrations of ATP are linked to macrophage death, we determined if this method of cell destruction also leads to reduced bacterial viability. We find that P2X7 is present on bovine macrophages from different sources, including both peripheral blood-derived as well as alveolar macrophages. In addition, P2X7 mRNA is present in B and T lymphocytes. The treatment of M. bovis-infected macrophages with ATP results in reduced macrophage viability as well as reduced M. bovis viability. 相似文献
20.
Cell adhesion molecules, leukocyte trafficking, and strategies to reduce leukocyte infiltration 总被引：6，自引：0，他引：6
Radi ZA Kehrli ME Ackermann MR 《Journal of veterinary internal medicine / American College of Veterinary Internal Medicine》2001,15(6):516-529
Leukocyte-endothelial cell interactions are mediated by various cell adhesion molecules. These interactions are important for leukocyte extravasation and trafficking in all domestic animal species. An initial slowing of leukocytes on the vascular endothelium is mediated by selectins. This event is followed by (1) activation of beta2 integrins after leukocyte exposure to cytokines and pro-inflammatory mediators, (2) adherence of leukocyte beta2 integrins to vascular endothelial ligands (eg, intercellular adhesion molecule-1 [ICAM-1]), (3) extravasation of leukocytes into tissues through tight junctions of endothelial cells mediated by platelet and endothelial cell adhesion molecule-1 (PECAM-1), and (4) perivascular migration through the extracellular matrix via beta1 integrins. Inhibiting excessive leukocyte egress and subsequent free radical-mediated damage caused by leukocyte components may attenuate or eliminate tissue damage. Several methods have been used to modify leukocyte infiltration in various animal models. These methods include nonspecific inhibition of pro-inflammatory mediators and adhesion molecules by nonsteroidal anti-inflammatory drugs (NSAIDs) and glucocorticoids, inhibition of cytokines and cytokine receptors, and inhibition of specific types of cell adhesion molecules, with inhibitors such as peptides and antibodies to beta2 integrins, and inhibitors of selectins, ICAMs, and vascular cell adhesion molecule-1 (VCAM-1). By understanding the cellular and molecular events in leukocyte-endothelial cell interactions, therapeutic strategies are being developed in several animal models and diseases in domestic animal species. Such therapies may have clinical benefit in the future to overcome tissue damage induced by excessive leukocyte infiltration. 相似文献